Leptin into the rostral ventral lateral medulla (RVLM) augments renal sympathetic nerve activity and blood pressure

Barnes and McDougal.Front. Neurosci.8:232.doi:10.3389/fnins.2014.0232.

Leptin is released from fat cells in order to promote satiety and increases energy expenditure. One mechanism by which leptin affects energy expenditure is by increasing sympathetic nerve  activity. Leptin signaling is mediated through the hypothalamus and has been shown to increase blood pressure and renal sympathetic nerve activity (RSNA).   we know that PVN sends projections to the RVLM and to the spinal cord to modulate sympathetic nerve activity. This study investigated if the leptin receptor is present in brainstem regions that control RSNA./For their anatomical studies they injected PRV into the  cortex of the kidney and did immunofluorescent staining for the leptin receptor (obrb). As for the functional studies they microinjected leptin and leptin receptor antagonist into the rvlm and recorded blood pressure and RSNA.  They found obrb positive cells in the C1/A1 region, VMM, caudal raphe and A5 area. Most of the PRV positive cells were found in the rostral portion of the RVLM (similar Nick’s paper) and found no difference between ipsilateral and contralateral RVLM.  They found that 65% of the C1/A1 region was double labeled.  As for the functional studies, they found that leptin lead to an increase in RSNA and BP. Injection of the antagonist prior to the leptin injection attenuated the BP and RSNA response.  Conclusion leptin release from fat cells is leading to increased energy expenditure via increasing sympathetic nervous system activity through activation of obrb receptors in the RVLM. MD